Hypersensitivity and its types ( type 1 anaphylaxis, type 2, Type 3, type 4 )
- 2. HYPERSENSITIVITY BY NOOR ARSHIA 5TH SEM BSC ( MICROBIOLOGY )
- 3. Hypersensitivity Refers to undesirable immune reactions produced by the normal immune system. It is an exaggerated immune response that results in tissue damage These reactions may be damaging, uncomfortable, or occasionally fatal.
- 4. It is a harmful immune response in which tissue damage is induced by exaggerated or inappropriate immune responses More harm is caused than good because of this over reaction. Even though hypersensitivity is often called ‘ ALLERGY’ , all allergies are not due to immune response and therefore are not HYPERSENTIVITIES
- 6. HYPERSENSITIVITY has two components PRIMING DOSE ( First dose ) SHOCKING DOSE ( Second dose )
- 8. HISTORY Prince of Monaco first observed the deleterious effects of jellyfish on bathers. Subsequently, Portier and Richet (1906) suggested a toxin to be responsible for these effects and coined the term “anaphylaxis”. Allergic rhinitis with symptoms of running nose reddening of eyes flushed face and disinterest in work was found to occur in Europe . This was identified as ‘HAY FEVER’ by John Bostock in 1829 which is known as ‘ALLERGY’ today Charles Blackley ( 1873) showed the role of pollen grain in Hay fever, and gave the name pollinosis.
- 9. Kutzner ( 1921 ) identified the role of immune system in allergy. humoral immunity – immediate hypersensitivity Cell- mediated immunity – delayed-type hypersensitivity. Depending on the time taken for the reaction and its mechanism, hypersentivity has been classified into immediate type and delayed type
- 10. Gell and Coombs (1963) classified hypersensitivity reactions into four categories . 1. TYPE I 2. TYPE II 3. TYPE III 4. TYPE IV
- 11. Types I, II, and III are antibody- mediated and are known as immediate hypersensitivity reactions, Type IV is cell-mediated (i.e., mediated by cell-mediated immunity) and is known as delayed hypersensitivity reactions.
- 12. TYPES OF ALLERGENS INGESTED ALLERGENS - Oral route Eg: sea foods, fruits,nuts,grains, and drugs such as aspirin etc INHALED ALLERGENS – Aeroallergens include pollen grains, animal dander, house dust, mites etc. INJECTED ALLERGENS – Includes various drugs such as antibiotics, hormones , insect venom, spider venom, and herion
- 15. TYPE I ( ANAPHYLACTIC ) HYPERSENSITIVITY Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity. ANAPHYLAXIS In Greek means ( ana – Against , phylaxis – Protection ) The reaction may involve skin (urticaria and eczema), eyes (conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues (asthma) and gastrointestinal tract (gastroenteritis).
- 17. The reaction may cause a range of symptoms from minor inconvenience to death. The reaction usually takes 15 - 30 minutes from the time of exposure to the antigen, Although sometimes it may have a delayed onset (10 - 12 hours). Mediated by IgE antibody to specific antigens The primary cellular component in this hypersensitivity is the mast cell or basophil. The reaction is amplified and/or modified by platelets, neutrophils and eosinophils. Mast cells stimulated and release histamine
- 19. ALLERGEN: Allergens are nonparasite antigens that can stimulate a type I hypersensitivity response. Atopy is the term for the genetic trait to have a predisposition for localized anaphylaxis. Atopic individuals have higher levels of IgE and eosinophils. Initial introduction of antigen produces an antibody response. More specifically, the type of antigen and the way in which it is administered induce the synthesis of IgE antibody in particular.
- 20. Immunoglobulin IgE binds very specifically to receptors on the surface of mast cells, which remain circulating. Reintroduced antigen interacts with IgE on mast cells causing the cells to degranulate and release large amounts of histamine, lipid mediators and chemotactic factors which cause smooth muscle contraction, vasodilation, increased vascular permeability, broncoconstriction and edema. These reactions occur very suddenly, causing death.
- 25. Diagnostic tests for immediate hypersensitivity include skin (prick and intradermal) tests , measurement of total IgE and specific IgE antibodies against the suspected allergens.
- 26. Type II hypersensitivity Type II hypersensitivity is also known as cytotoxic hypersensitivity and may affect a variety of organs and tissues. The antigens are normally endogenous, although exogenous chemicals (haptens) which can attach to cell membranes can also lead to type II hypersensitivity. Drug-induced hemolytic anemia, granulocytopenia and thrombocytopenia are such examples. Penicillin allergy also belong to this class.
- 27. The reaction time is minutes to hours. Type II hypersensitivity is primarily mediated by antibodies of the IgM or IgG classes and complement . Phagocytes may also play a role. The lesion contains antibody, complement and neutrophils. Rh factor incompatibility IgG Abs to Rh an rbc antigen › Rh+ baby born to Rh- mother during first pregnancy time will be fine. But 2nd pregnancy can have Abs to Rh from 1st pregnancy. ›Ab crosses placenta and baby kills its own rbcs. › Treat mother with Ab to Rh antigen right after birth and mother never makes its own immune response.
- 31. Type III hypersensitivity Immune complex type Due to formation of Antigen antibody immune complexes. IgG mediated ( instead if IgE or IgM ) Large amount of antigen and antibodies form complexes in blood. This complexes If not eliminated can deposit in capillaries or joints and trigger inflammation.
- 32. The reaction may be general (e.g., serum sickness) or may involve individual organs including Skin (e.g., systemic lupus erythematosus, Arthus reaction), Kidneys (e.g., lupus nephritis), Lungs (e.g., aspergillosis), Joints (e.g., rheumatoid arthritis) or Other organs. This reaction may be the pathogenic mechanism of diseases caused by many microorganisms.
- 33. Macrophages bind to immune complexes via FcR and phagocytize the complexes. BUT If unable to phagocytize the immune complexes can cause inflammation via C’ activation ---> C3a C4a, C5a and "frustrated phagocytes".
- 36. It is called DTH because the response is Delayed Reaction involves sensitized T cells and release of its lymphokines as mediators and amplifiers Mediated by cells rather than antibodies Clinical states: Contact dermatitis, , Transplant rejection, Granuloma Type IV hypersensitivity Delayed Type hypersensitivity ( DTH )
- 37. Th1 cells release cytokines to activate macrophages causing inflammation and tissue damage. Continued macrophage activation can cause chronic inflammation resulting in tissue lesions, scarring, and granuloma formation. Response starts after 48 -72 hrs
- 39. MECHANISM
- 43. ECZEMA
- 44. TREATMENT OF ALLERGIES DESENSITIZATION THERAPY
- 46. SUMMARY